Abstract

Primarily on the basis of epidemiological evidence, Helicobacter pylori was classified as a definite human carcinogen in 1994. Although several pathophysiological consequences of chronic H. pylori gastritis have been identified which may contribute to the development of gastric carcinoma, it is still largely unknown why only a minority of individuals infected with H. pylori (approximately 1/1000) develop this fatal disease. In recent years many studies have examined potential risk factors of H. pylori gastritis to improve our understanding of the early events in gastric carcinogenesis. The present paper summarizes research data supporting the following hypotheses: (a) Some H. pylori possess virulence factors which may contribute to the pathogenicity of the organism and may increase the risk for subsequent severe gastroduodenal diseases such as gastric cancer. However, the associations between these virulence factors and disease is not specific, and may vary considerably among different geographic regions. (b) Chronic H. pylori gastritis induces several pathophysiological alterations which may promote cancer development. In particular, the corpus-dominant phenotype of H. pylori gastritis is strongly associated with gastric cancer. (c) A family history of gastric cancer per se, but also in combination with H. pylori infection, is associated with histopathological and molecular alterations that are considered relevant in gastric carcinogenesis.

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